TL;DR
The findings define the cellular trajectories of neurodegeneration in CS, and identify convergent endolysosomal, mitochondrial, and inflammatory mechanisms that support a broader role for endolysosomal dysfunction in Alzheimer’s disease pathogenesis.
Abstract Katanins are microtubule-severing ATPases. Dysfunction of katanin subunits has been implicated in impaired neurogenesis, morphogenesis, and neuronal migration. Although heterozygous variants in KATNAL2 (katanin-like 2), a known autism-spectrum disorder (ASD) risk gene, have been reported in patients with ASD o...
The mechanisms underlying type 2 diabetes-associated cognitive dysfunction (DACD) remain poorly understood, hindering therapeutic progress. Here, we integrated spatial transcriptomics and single-nucleus RNA sequencing to delineate the spatiotemporal molecular and cellular landscape of DACD in brain tissues from 3- and...
It is shown that depletion of these AD risk genes disrupts baseline morpho-transcriptomic coupling and fundamentally alters microglial phagocytic capacity, revealing how AD GWAS genes may drive microglia into dysfunctional states characterized by altered morphology, distinct multi-omic signatures, and impaired function...
Overall, MA-5 suppresses neuroinflammation and reverses accelerated transcriptomic aging, supporting its potential as a therapeutic strategy for GD and other lysosomal storage disorders, as well as for diseases characterized by mitochondrial dysfunction, chronic inflammation, and pathological accumulation.
Microglia-regulated neuroinflammation is associated with major depressive disorder (MDD), yet the molecular drivers of pathological microglia-neuron interactions remain poorly defined. Here, we conducted single-nucleus RNA sequencing (snRNA-seq) of the prefrontal cortex (PFC) in mice susceptible to chronic social def...
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